Neuropathology 1: CVD Flashcards

1
Q

name the 3 types of glial cell

A

astrocytes - most prevalent
oligodendrocytes
ependymal cells

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2
Q

ependymal cells line..

A

the ventricular system

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3
Q

what is the pathological cellular response seen in stroke?

A

rapid necrosis with sudden acute functional failure

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4
Q

what kind of neuronal damage occurs as a result of hypoxia?

A

acute neuronal injury with irreversible shrinking and angulation of nuclei, loss of the nucleolus and a RED cytoplasm

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5
Q

when does acute neuronal injury occur in relation to the time of injury

A

12-24 hours after injury

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6
Q

name the axonal reaction to injury?

A

increased protein synthesis

degeneration of myelin sheath and axons distal to injury

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7
Q

what does chronic degeneration of a neuron look like?

A

shrunken, angulated and lost neurons
small dark nuclei
neuronal tissue replaced by reactive gliosis

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8
Q

small dark nuclei are an example of what damage?

A

chronic damage

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9
Q

what are inclusions? what are they common in?

A

subcellular alterations common in neurodegenerative conditions eg alzheimers and in aging

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10
Q

oligodendrocytes are sensitive to ___ damage

A

oxidative

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11
Q

damage to the myelin sheath poses what risks?

A

conduction reduced

axons exposed to injury

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12
Q

damage to what cells is a feature of demyelinating disorders

A

oligodendrocytes

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13
Q

star shaped cells with multipolar cytoplasmic processes describe….

A

astrocytes

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14
Q

what do the cytoplasmic processes of astrocytes do?

A

envelop synaptic plates

wrap around vessels and capillaries of the brain

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15
Q

what cells are responsible for reabsorbing and recycling glutamate?

A

astrocytes

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16
Q

what pathological process is the main indicator of CNS injury?

A

gliosis

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17
Q

describe gliosis

A

astrocyte hyperplasia and hypertrophy
prominent nucleolus
small dark nuclei

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18
Q

describe the role of M1 microglia

A

anti-inflammatory, phagocytic, for acute injury

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19
Q

describe the role of M2 microglia

A

pro-inflammatory, for chronic injury

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20
Q

which type of microglia is for chronic injury

A

M2

21
Q

what happens to microglia when theyre injured?

A

they proliferate, are recruited via inflammatory mediators and form aggregates around necrotic tissue

22
Q

most common cause of nervous system injury?

A

hypoxia

23
Q

the brain consumes __ % of the body’s total oxygen

A

20

24
Q

describe the process of excitotoxicity

A

energy failure in the cell results in degradation of the mP -> glutamate released but not reabsorbed well -> severe excitation -> Ca excess

25
Q

excess Ca as a result of excitotoxicity has what consequences?

A

oxidative stress
apoptisis
mitochondrial dysfunction
protease activation

26
Q

what happens in cytotoxic oedema? what can it lead to?

A

excess Na and Cl in the cell cause water to move into the cells across the BBB causing ionic oedema

27
Q

vasogenic oedema occurs in what brain pathologies?

A

trauma, tumours, inflammation

encephalopathy

28
Q

the brain receives __% of the cardiac output

A

15

29
Q

global hypoxic ischaemic damage can occur in the context of…

A

generalised reduction in perfusion/oxygenation
cardiac arrest
severe hypotension

30
Q

focal hypoxic ischaemic damage can occur in the context of…

A

vascular obstruction

31
Q

what parts of the brain are more susceptible to ischaemic damage?

A

areas between arterial territories

32
Q

neurons are more sensitive than glial cells to hypoxic ischaemic damage T or F

A

T, especially purkinje cells in the cerebellum

33
Q

what kind of infarctive stroke is most common?

A

thrombotic

34
Q

most common area for a thrombotic infarctive stroke

A

middle cerebral artery

35
Q

where do cardioemboli tend to arise from?

A

internal carotids
aorta
heart

36
Q

after 12-24hrs of cerebral infarction what does the brain look like microscopically?

A

red neurons, oedema

37
Q

what becomes the predominant cell type -14 days after a cerebral infarction?

A

microglia

38
Q

when does gliosis begin after a cerebral infarction

A

1 week

39
Q

when does a gliotic scar appear after a cerebral infarction

A

after a few weeks

40
Q

clinical presentation of a middle cerebral artery occlusion

A

weakness in contralateral face and arm

41
Q

what is arteriolosclerosis

A

thicker, stiff, weaker arterioles

42
Q

lacunar infarcts occur from occlusion of….

A

small penerating arteries

43
Q

clinical presentation of hypertensive encephalopathy?

A

severely hypertensive

symptoms of raised ICP

44
Q

pathological findings of hypertensive encephalopathy?

A

arteriolar fibrinoid necrosis
petechiae
tentorial and tonsillar herniation
global cerebral oedema

45
Q

what does amyloid do to BVs

A

thins their walls making them more likely to rupture

46
Q

most likely area for an intracerebral haemorrhage

A

in basal ganglia

47
Q

most common cause of subarachnoid haemorrhage?

A

berry aneurysm rupture

48
Q

most common area of berry aneurysms?

A

around arterial bifurcations arising from the cirle of willis
in territory of internal carotid

49
Q

complications of subarachnoid haemorrhage

A

infarcts in brain parenchyma
intracerebral haematomas
hydrocephalus